Acute impaction of the rumen
Rumen overload-rumen acidosis

Definition:

 Ingestion of large amounts of highly fermentable carbohydrate feeds causes:
1) Acute illness due to the excess production of lactic acid.
2) Clinically the disease is manifested by severe toxemia dehydration, recumbency, complete ruminal stasis and high mortality rate.


Causes:
1) Ingestion of large quantities of highly fermentable carbohydrate whole or ground grains.
2) Sudden change of the ration.
3) Excessive feeding especially during dry season where high percent of fermentable carbohydrates will be eaten.


Pathogenesis:

 Rapid fermentation of the carbohydrate by the Gram-positive cocci usually Strept. Bovis causes the formation of large quantities of lactic acid, which increase the osmotic pressure into the rumen leading to dehydration and Haemoconcentration accompanied by anuria. Rumen motility decreases as pH falls, Rumen stasis occurs Rumen microflora are destroyed and replaced by lactobacilli and streptococci bacteria.
- There is severe depression of volatile fatty acids production due to the destruction of the ruminal bacteria and protozoa.
- Histamine production occurs which leads to laminitis.
- Bacterial infection leads to the development of metastatic abscesses in the liver with subsequent formation of hepatitis which may be symptomless.
- Necrosis and gangrene may affect the forestomachs and may lead to acute diffuse peritonitis and toxemia ending by death.


Clinical findings:
1- The sings varies with the nature and the amount of the feed, being faster with ground food than the whole grains.
2- The first sign may be abdominal pain with kicking at the belly.
3- There is profound depression and desclination to move.
4- Respiration is increased in rate and may be accompanied by grunting.
5- Anorexia is complete and affected animals usually do not drink much water.
6- Distention of the abdomen and slight Ruminal tympany (may not be marked).
7- Palpation on the left paralumbar fossa reveals a firm and doughy material.
8- Nose is dry and mucopurulent exudate accumulates in the nostrils.
9- Grinding on the teeth.
10- Diarrhea with the passage of soft or watery faeces is seen.
11- In severe cases there may be profuse diarrhoea accompanied by the passage of much mucus and some blood.
12- Increase in pulse rate up to 120-140/min and the pulse is weak.
13- Temp is below normal.
14- Ruminal movements are completely absent but gurgling sounds of gas may be heard (accumulation of fluids).
15- Animals gragger and appear to be blind; and the eyes have not eye preservation reflex.
16- Laminitis and recumbency may follow after 48 hrs but in may be an early sign when animals lie, they are often with the head turned into the flank (resembles parturient paresis).
17- Death occurs in 24-72 hrs in most fatal cases. Return of normal ruminal movements, pulse rate, Passage of large amounts of soft feces may indicate a phase toward recovery.
18- Some animals may appear to have a temporary improvement but become severely ill again on the 3rd and 4th day.
Death may follow because of diffuse peritonitis.
N.B.: The above signs are seen in severe cases-but as mentioned above it varies according to the type of feed and its amounts.

 

Clinical pathology:


1- Measurement of Haematocrite (PCV) may rise up to 50 or 60 (Normal 30-31%).
2- Blood pressure falls.
3- Urine pH falls, Oliguria may follows with anuria.
4- Blood glucose and phosphates levels rise.
5- Blood glucose and phosphate levels are elevated.
6- pH of the ruminal fluid falls: 4.5 - 5 (Moderate) less than 4.5 (severe).
7- Motility of inifisoria (microflora) disappear.
8- Gram positive microflora appears.
9- A degree of proteinuria is noticed.


Diagnosis:

 
- History of engorgement with grains when this is not available the disease may resemble parturient paresis and can be differentiated as follow:
- Parturient paresis: are seen in recently calved or in late pregnancy or in early lactation. There is no peripheral circulatory collapse + heart rate is not greatly increased and feces are hard and dry.
Differential diagnosis from the following condition:

 

 

Acute hepatic insufficiency:

accompanied by blindness and staggering gait but there is usually jaundice and heart rate is approximately normal.


Arsenic poisoning:

 Enteritis is more severe and death is quicker.


Lead poisoning:

 Is manifested by severe nervous signs. In both lead and arsenic poisoning, faecal analysis should be adopted.


Enterotoxaemia:

 Caused by Cl. perfringens type D that may occur in well fed calves and lambs and could be diagnosed on the basis of the toxicity of bowel filtrates.


Early stages of traumatic reticuloperitonitis:

 Here there is severe pain on abdominal percussion and changes in the white cell count.


Treatment:


1) Mild cases could be treated as in simple indigestion.
2) Prevent access to further eating of grains.
3) Exercise vigorously for half an hour 3 times daily.
4) Allow water but in limited quantities at time.
5) Inject antihistaminics.
6) Give oral antibiotics.
7) Give alkaline purgatives.
There are the broad lines of treatment.


Prescriptions:


- Magnesium hydroxide or Mag. carbonate to be given 250-500 grams as an initial dose followed by 120 gm at 12 hrs intervals.
- Oral penicillin: from .0.5 - 1.0 million for sheep orally. These restrict the growth of bacteria, which produce lactic acid. In cattle higher doses are given up to 10 million I.U.
- Oral tetracyclines: 5 - 10 grams and repeat it at 12 hrs intervals.
- Repair the dehydration by injection of large quantities of isotonic solutions 4 - 10 litre.
- Repair the acidosis by the (i/v) injection of 500 ml 2.5% solution of sod bicarbonate. -- Inject slowly and watch the animal if you repeat the dose otherwise alkalosis may develop, oral doses may be safer (120 gm twice a day).
- Injection of thiamine 2 - 4 grams is excellent in such cases, or bakers yeast 500 gm daily given per os.
- Ca. borogluconate is said also to help recumbent animals.
- Emergency rumenotomy should be performed in serious cases and the rumen should be washed out. The contents should be replaced by mixture of hay + some water + rumen transplants or 1-2 litre of fresh ruminal fluid gained from healthy individuals.


Prevention:


1- Gradual changes of the ration when start feeding on grains until adaptation of the new diet over a period of 6 days.
2- The addition of alkalinizing agents to the ration of beef cattle fed heavily on grain to the level of 7% with a mixture of ground limestone and sod. Bicarbonate.


 Ruminal tympany (Bloat)

 

Def: Over- distension of the rumen and reticulum with gases, either free or mixed with the ingesta. The incidence of the disease has increased with the heavy application of fertilizers.

 

 

 

Aetiology:

Primary Ruminal tympany:

a) Dietary factors:

 

1- Grassing on very succulent pasture, particularly young rapidly growing legumes in the pre-bloam stage (the important cause).

2- May also occurs when cattle grassing on cereal crops; cabbages, leguminous vegetable crops (peas-beans) young grass pasture with a high protein content.

 

 

 b) Animal factors:

 

1- Cattle vary in their susceptibility to tympany perhaps due to hereditary factors.

2- Foaming of the ruminal contents:

Foaming of the Ruminal contents produced by the high viscosity or surface tension. This is caused by:

- The pH of the rumen is an important factor to make the foam stable. Stability occurs at a pH of about 6.0 the composition of the rumen diet and the activity of the microflora influence this factor (pH).

- The rate of flow and composition of the salvia has an effect on the tendency for a tympany to occur as saliva act as a buffer on the pH of the rumen. Salivary mucin prevents the formation of foam but the mucinolytic bacteria in the rumen may destroy the mucin and permit bloating. The amount of saliva may dilute the ingesta. The low amount of saliva may increase the susceptibility of cows to develop tympany.

- An increase in slime producing bacteria may be the cause of foaming (frothiness) as these microorganisms produce polysaccharides, which encourage froth formation. Moreover, this bacteria digest plant lipids which have an anti-foaming effect.

 

 

Secondary Ruminal tympany:

 

1) Physical obstruction: This prevents eructation and is caused by foreign body stenosis-pressure from enlargements outside the esophagus or obstruction inside the esophagus or at the cardia.

2) Vagus indigestion and diaphragmatic hernia: These interfere with oesophageal function and cause chronic tympany. The condition may occur in tetanus in young lambs due to spasms of the oesophageal musculature.

3) Interference with the nerve pathways:

These are responsible for maintenance of eructation reflex. The receptor organs in this reflex are capable to differentiate between gas and foam liquid lesions of the vagus nerve may interrupt the reflex action, which is important to remove gas from the rumen.

4) Atomy in normal tone of the musculature of the rumen and reticulum. Sudden change in pH either to acidity or alkalinity may cause such atony.

5) Persistent or enlarged thymus may cause chronic tympany in calves up to 6 months.

  

Pathogenesis:

 

1) Free gas ruminal tympany is due to oesophageal obstruction or atony.

2) Frothiness of the ruminal contents causes the obstruction of the cardia and this inhibits the eructation reflex consequently cranial sphincter of the esophagus fails to open. Rumen movements are stimulated by distension causing hypermotility which increase frothiness and terminally there is loss of muscle tone and motility.

 Clinical findings:

Primary pasture bloat:

 

Which appears clearly in the upper left flank in the form of:

1) Obvious distension of the rumen, which occurs suddenly 15 minutes.

2) Discomfort and the animal may get up and lie down, frequently kicks at the belly and even roll.

3) Dyspnoea is marked which characterized by mouth breathing, protrusion of the tongue, salivation and extension of the head.

4) Respiratory rate is increased up to 60 min.

5) Projectile vomiting may occur and the faeces may be expelled in a stream.

6) Ruminal movements are at first increased but later on the sounds are reduced in volume. When the distension is severe, the movements are decreased or completely absent.

7) Percussion produces tympanic sound allover the rumen.

8) In acute stages rumination and eructation disappear (may increase before clinical signs).

9) Pulse rate is increased up to 100-120.

10) Death occurs due to:

a- The absorption of the toxic gases (H2S, toxic amines, histamine).

b- Depression of the cardiovascular, respiratory systems. Death can occur within 3-6 hours from the onset of the clinical signs.

 

Secondary bloat:

1) There is excess of free gases on the top of the ruminal contents.

2) As in pasture bloat there is usually an increase in rate and force of ruminal movements in the early stages followed by atony.

 3) Passage of the stomach tube or trocarization induce the expulsion of large quantities of gas and the retention subsides. (Also by the stomach tube you can detect if there is oesophageal obstruction).

4) Pulse is increased; systolic murmur is often audible which may be due to displacement of the diaphragm and distortion of the base of the heart.

 

 

Diagnosis:

 

Simple in primary bloat but the difficulty in secondary bloat especially when the bloat is chronic. Passage of the stomach tube will detect the oesophageal obstruction or stenosis. Vagus indigestion and diaphragmatic hernia may have a previous history of traumatic reticuloperitonitis and partial anorexia.

- Tetanus is manifested by limb rigidity, prolepses of the third eyelid and hyperethesis.

- Carcinoma and papilloma of the oesophageal groove and reticulum are difficult to be diagnosed without rumenotomy.

 

Treatment:

1) Treatment of the secondary tympany depends upon the removal of the cause.

2) In any form adopt the first aid to save the animal.

a- Tying a stick in the mouth.

b- Let the animal to stand with the front feet raised.

c- Drench with non-toxic vegetable oil or mineral oil

d- Smear the back of the tongues with wood tar.

3) Passage of the stomach tube to relief gases, and in emergency cases trocarization must be performed.

 

 

Primary bloat:

The aim in this type is to reduce the stability of the foam by:

1) Oral administration of any vegetable or mineral oil (300-800 ml) for large animals and 60-100 ml for sheep, oils could be mixed with a detergent. A stomach tube to avoid aspiration and to remove excess free gas could administer this.

2) Oral administration of poloxalene (25-50 gm) to reduce stability of the foam.

3) In severe cases trocarization should be adapted and oils can be introduced through the cannula by a syringe with a long nozzle.

4) Turpentine oil (30-60 ml) reduces the viscosity of the foam.

5) Purgatives may be administered with the oil to facilitate evacuation of the tympany-produced ingesta.

6) Anti-histaminics may be recommended but their use in frothy bloat may have a dangerous effect.

7) Severe cases may need rumenotomy.

8) Secadine (Anti bloat drug).

 

 Vagus Indigestion

It is usually seen in cattle and buffaloes and is characterized by:

- Delayed passage of food in the intestine due to paralysis of stomachs.

- Distension.

- Anorexia.

- Passage of soft pasty faeces in small quantities. Caused by lesions, which involve the vagus nerve supply to the forestomachs and abomasums.

 

Causes:

1) The commonest cause is traumatic reticulo-peritonitis.

2) Scar tissue lesions affecting the ventral branch of the vagus nerve, which ramifies over the anterior wall of the reticulum.

3) Lesions, which prevent oesophageal, groove reflexes or which cause adhesions between rumen and abomasums.

4) Actinobacillosis of the rumen and reticulum may act also as a cause.

5) Involvement of the vagus nerve as a result of enlargement of L.N. due to tuberculosis or lymphomatosis. Similar disturbances may occur as a result of diaphragmatic hernia.

6) In sheep’s peritonitis caused by sarcosporidia and cysticercus tennicollis.

 

Pathogenesis:

1) Varying syndromes depending upon the affected branches of the nerve and to the varying degrees of immobilization caused by adhesions of reticulum to diaphragm this leads to: Development of achalasia of the reticulo- omasal and pyloric sphincters which result in accumulation of food material in the rumen.

2) Failure of the oesophageal groove to permit the passage of food into the rumen may accompany pyloric achalasia.

 

Clinical findings:

3 major syndromes.

1) Distension of the rumen with hypermotility:

- This is not related to pregnancy or parturition.

- Moderate to severe ruminal tympany although the animal did not eat with strong continuous movement of the rumen.

- The faeces are normal or pasty but scanty.

- No fever.

- Heart rate is usually slower than normal and sounds are accompanied by systolic murmurs, which wane with respiration being loudest at the peak of inspiration. This disappears when tympany is relieved.

 

 

II - Ruminal distension the atony:

- This occurs in late pregnancy and may persist after calving. The cow is clinically normal but does not eat well.

- Cow passes only small amount of faeces - soft and pasty.

- Tympany does not respond to treatment.

- Ruminal movements are seriously reduced or absent.

- No fever, no pain on percussion of the abdomen.

- Rectal palpation may reveal a distended rumen to the •extent that it blocks the pelvic inlet.

- Animal losses weight rapidly and become very weak and eventually recumbent. At this stage heart rate is increased and the animal dies from inanition.

 

 

III Pyloric obstruction:

- Most cases of this type occur in late stage of pregnancy.

- Anorexia and reduced volume of pasty faeces.

- No obvious abdominal distension and no systemic reaction until the late stages when the pulse rate rises rapidly.

- There is a distension of the abomasums and you can palpate it on the floor of the abdomen on rectal examination (but this is impossible when the cow is pregnant). The abomasums is firm and not distended with gas or fluid.

- Rumen movements are completely absent and death occurs slowly due to inanition.

 

 

Remarks:

 

Combination of these types may occur especially distension of the rumen combined with abomasal obstruction.

  

P.M. Findings:

 

1) Firm distended abomasums half filled with digested fibers and the rest is filled as that of the rumen contents.

2) Ulcers in mucosa.

3) Intestine may be empty.

4) Lesions (adhesions) in the reticulum may suggest a history of traumatic reticulo-peritonitis.

 

 

Clinical pathology:

 Moderate neutrophilia + neutrophilic shift to the left relative monocytosis which reflects chronicity.

Diagnosis: (Differential diagnosis)

Indigestion due to:

1) Left abomasal displacement:

a- There is audible abomasal sounds.

b- Left lower flank of the abdomen is sunken rather than distension.

c- Ruminal movements are not absent or exaggerated but the sounds are modified.

2) Chronic reticulo-peritonitis - impossible to differentiate this from vagus indigestion unless without rumen atony.

3) Subacute abomasal torsion (Right displacement): here the distended abomasums can be palpated filling the right half of the abdominal cavity.

4) Lipoma or fat necrosis, causing partial obstruction of the intestine could be palpated by rectal palpation.

 

 Treatment:

 

- Rumenotomy and empty of rumen may be followed by slow recovery over a period of 7-10 days when there is hypermotility.

- Abomasotomy is not recommended as the motility of the abomasums does not return to normal.

- Conservative treatment has no good effect.

- Slaughtering is recommended.